Abstract

The present project studies the effects of chemical lesioning in the dorsal medulla (DM) or rostral ventrolateral medulla (RVLM) on glutamate-induced cardiovascular action of the pontine gigantocellular tegmental field (PFTG) and lateral tegmental field (PFTL) in cats. Experiments were performed on 39 adult cats anesthetized with intraperitoneal injection of a mixture of alpha-chloralose and urethane. Systemic arterial blood pressure (SAP), heart rate (HR) and vertebral nerve sympathetic activity (VNA) were continuously monitored. Microinjections of the glutamate solution (Glu, 0.25 M of sodium glutamate dissolved in artificial cerebrospinal fluid with 0.5% pontamine sky blue) in 50- to 70- nl aliquots were made in the PFTG and PFTL. SAP, HR, and VNA were measured before and after chemical lesioning of the DM and/or RVLM and compared. The DM or the RVLM was lesioned by injection of 150-200 nl of kainic acid (24 mM) acutely. We found that when the ipsilateral DM was lesioned, microinjection of Glu into PFTG no longer elicited a pressor response. In contrast, when the contralateral DM was lesioned, the Glu-induced PFTG pressor response was little affected. Lesioning of either the ipsi- or contralateral RVLM affected the PFTG response very little. This suggests that the connection between PFTG in producing the pressor action is principally unilateral through the ipsilateral DM. When the ipsi- or contralateral DM was lesioned, injection of Glu into the PFTL no longer could elicit a depressor response. Interestingly, when either the ipsi- or contralateral RVLM was lesioned, the PFTL-induced depressor effect changed to a pressor one. These results suggest that the PFTL depressor effect is dependent on the integrity of both the DM and RVLM. Furthermore, there may be a mixture of sympathoexcitatory and parasympathoexcitatory neurons in the PFTL.

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